Araneo B A, Dowell T, Diegel M, Daynes R A
Division of Cell Biology and Immunology, University of Utah School of Medicine, Salt Lake City.
Blood. 1991 Aug 1;78(3):688-99.
The present study examined the effects of the androgen steroid, dihydrotestosterone (DHT), on murine T-cell production of a number of lymphokines. Direct exposure of murine T cells to DHT in vitro was found to reduce the amount of interleukin-4 (IL-4), IL-5, and gamma-interferon (gamma IFN) produced after activation with anti-CD3 without affecting the production of IL-2. Exposure of T cells to either androstenedione or testosterone (the metabolic precursors of DHT) affected no change in the biosynthesis of either of these lymphokines. We have determined that macrophages possess 5 alpha-reductase, and are thus competent to metabolize testosterone to DHT. This physicochemical information is complemented by a functional analysis of macrophage metabolism of testosterone. By incubating bone marrow macrophages with testosterone, before their use as accessory cells, the IL-4 and IL-5 producing potential of the activated T cells cocultured with them was depressed. That the observed effect was mediated by the conversion of testosterone to DHT was further corroborated by illustrating that the inhibition of IL-4 production was abrogated if 4MA, a specific 5 alpha-reductase inhibitor, was added to macrophage cultures containing testosterone. The biologic role of DHT in lymphokine and immune response regulation in vivo was addressed using several lines of investigation. First, transdermal delivery of DHT to groups of mice altered the capacity of T cells residing in the draining lymph nodes, only, to produce lymphokines. Second, treatment of either aged mice or the T cells isolated from them with a combination of dehydroepiandrosterone and DHT restored the capacity of their T cells to produce IL-2, IL-4, and gamma IFN to levels equivalent to that of younger mice. Finally, we observed a difference between males and females of a given age to produce IL-2, IL-4, and gamma IFN, with both IL-4 and gamma IFN production being elevated in females. Collectively, our findings indicate that DHT, similar to other steroid hormones, may play an important role in lymphokine regulation in vivo.
本研究检测了雄激素类固醇双氢睾酮(DHT)对小鼠T细胞产生多种淋巴因子的影响。研究发现,在体外将小鼠T细胞直接暴露于DHT可减少抗CD3激活后产生的白细胞介素-4(IL-4)、IL-5和γ干扰素(γIFN)的量,但不影响IL-2的产生。将T细胞暴露于雄烯二酮或睾酮(DHT的代谢前体)中,这些淋巴因子的生物合成均未发生变化。我们已经确定巨噬细胞具有5α-还原酶,因此能够将睾酮代谢为DHT。这一物理化学信息通过对巨噬细胞睾酮代谢的功能分析得到补充。在用骨髓巨噬细胞作为辅助细胞之前,将其与睾酮一起孵育,与之共培养的活化T细胞产生IL-4和IL-5的潜力会受到抑制。如果向含有睾酮的巨噬细胞培养物中添加特异性5α-还原酶抑制剂4MA,IL-4产生的抑制作用被消除,这进一步证实了观察到的效应是由睾酮转化为DHT介导的。使用多种研究方法探讨了DHT在体内淋巴因子和免疫反应调节中的生物学作用。首先,将DHT经皮递送至小鼠组,仅改变了引流淋巴结中T细胞产生淋巴因子的能力。其次,用脱氢表雄酮和DHT联合处理老年小鼠或从它们分离出的T细胞,可将其T细胞产生IL-2、IL-4和γIFN的能力恢复到与年轻小鼠相当的水平。最后,我们观察到给定年龄的雄性和雌性在产生IL-2、IL-4和γIFN方面存在差异,雌性的IL-4和γIFN产生均升高。总体而言,我们的研究结果表明,与其他类固醇激素类似,DHT可能在体内淋巴因子调节中起重要作用。